Fatty liver - fatty liver

Fatty liver - fatty liver

    * Introduction
    * Causes
    * Signs and symptoms
    * Diagnosis
    * Treatment
Fatty liver is excessive accumulation of lipids in hepatocytes, the response most frequently in liver injury. There are two types of the alcoholic steatosis and non-alcoholic. Alcoholic and nonalcoholic fatty liver disease are the major causes of death, the progression to cirrhosis and liver failure. Fatty liver inflammation called steatohepatitis, and may occur in alcohol-free or non-alcoholic steatohepatitis.
Non-alcoholic fatty liver disease is a syndrome that develops and produces non-alcoholic patients liver lesions are not histologically distinguishable from the alcohol. Most often occurs in middle-aged women, overweight, diabetes or elevated triglyceride levels in the blood. May also occur in some pregnant women suffering from preeclampsia. Most patients are asymptomatic. Those who have symptoms, they include: fatigue, malaise and right upper quadrant abdominal pain. Hepatomegaly occurs in 75% of them. The prognosis is controversial. Many of the patients will develop liver failure or cirrhosis, however, some cytotoxic drugs and metabolic disorders are associated with progression steatohepatitei.
Alcoholic fatty liver disease is a consequence of chronic alcohol ingestion for long periods of time. It is a combination of fatty liver, liver inflammation and necrosis spread in varying degrees. Signs and symptoms are similar to those of non-alcoholic form. The prognosis is determined by graders fibrosis and inflammation. Without the presence of fibrosis, fatty liver is completely reversible in 6 weeks, if alcohol is stopped. Excessive fibrosis and its complications: cirrhosis, ascites, liver failure, esophageal bleeding and hepatic encephalopathy are severe and irreversible. Abstinence is based therapy can prevent progression of steatosis and prolong life.
Pathogenesis
The two clinical entities showing the same pathogenic mechanisms: Increased hepatic uptake of fatty acids The level of fatty acids by the liver increases significantly captured immediately after consuming alcohol or obese persons with hyperlipidemia. Alcohol increases the uptake of fatty acids by increasing portal blood flow and independently, by altering the structure of membrane lipids in hepatocytes. Blocking fatty acid oxidation Alcohol and lipids inhibit excessive hepatic acid oxidation by inhibiting mitochondrial oxidation and tricarboxylic acid cycle. Blocking transport fatty acids into mitochondria Transport of free fatty acids from cytosol to mitochondria is required for beta-oxidize. Transport is mediated by an enzyme from the mitochondrial membrane surface-transferase carnitinpalmitoil. Chronic alcoholism has been shown to reduce the activity of this enzyme, but also through increased production of malonyl Co-A by inhibiting the enzyme activity of malonyl Co-A decarboxylase. Accelerating production of de novo fatty acids, triglycerides and increase their esterificarii excretion decreased liver tricliceride are other mechanisms involved. Macroscopic liver histological sections is yellow, with large bubbles to the surface fat, brittle and increased volume. Microscopic macroveziculare shows accumulation of fat droplets in appearance, which marginalizes the nucleus. Microveziculele fat mitochondria are destroyed.